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101.
目的探讨环氧化酶-2(C0X-2)在预测经尿道膀胱肿瘤电切术(TURBT)后肿瘤复发中的作用。方法收集52例行TURBT治疗的膀胱肿瘤患者资料,采用免疫组化方法检测肿瘤组织标本中COX-2的阳性表达,分析其与患者临床病理资料以及术后随访资料间的相关性。结果 52例标本中COX-2阳性表达30例,术后平均随访28.6个月,复发9例。COX-2阳性表达率与肿瘤T分期明显相关(P0.05),与患者年龄、性别、病理G分级、单/多发病灶之间没有相关性,单因素分析显示膀胱肿瘤术后复发与临床T分期(P0.01)、单/多发病灶(P0.05)密切相关,而与COX-2阳性表达率、肿瘤G分级、性别没有相关性。结论 COX-2作为TURBT术后肿瘤复发的预测因子及其具体机制有待进一步研究。  相似文献   
102.
目的 评价重组人红细胞生成素 (rhEPO)、重组人粒细胞集落刺激因子 (rhG CSF)对芥子气全身吸收中毒犬的治疗效果。方法 以成年家犬为中毒模型 ,共 10条 ,中毒剂量为 12mg kg,皮下注射。随机分为中毒对照组 4条 ,治疗组 6条 ,治疗组动物在中毒后 30min即进行相应的药物治疗。中毒前所有犬各测一次血常规的基础值 ,中毒后每日监测血常规的动态变化 ,持续 1周。结果 对照组犬于 3天内死亡 3条 ,治疗组犬全部成活。对照组白细胞计数 (WBC)在中毒后第 3开始剧烈下降 ,红细胞计数 (RBC)在中毒后即有轻度上升 ,之后回落 ;而治疗组WBC、RBC在中毒后 1周内均无显著变化。两组的淋巴细胞计数 (LYM)在中毒后都有显著下降 ,治疗组稍好于对照组。治疗组的网织红细胞计数 (RC)于中毒后第 2天开始显著增长 ,之后维持在高水平 1周左右。治疗组的RC变化不明显。结论 犬芥子气中毒后 ,应用rhEPO、rhG CSF能明显改善中毒犬的部分血常规指标  相似文献   
103.
广州医疗服务满意度现况初步调查   总被引:11,自引:6,他引:11  
目的 了解广州市民对医疗服务的满意情况。方法 用调查问卷的方式在广州市调查642人。结果 69.2%的人对总的医疗服务质量满意,大部分人认为医生的医术水平是可以依赖的,选择小医院就诊的比例较高。“红包”现象和医疗纠纷依然存在。结论 文化程度和等候时间是医疗服务满意度的影响因素。  相似文献   
104.
鼻灌洗在职业和环境医学中的应用   总被引:2,自引:0,他引:2  
鼻灌洗(nasallavage,NAL)是一种简便易行的检查方法,它可客观地反映呼吸系统的病理生理变化。由于NAL没有创伤性,可重复检查,因此特别适合于现场研究和以儿童作为研究对象的调查。自本世纪90年代以来,许多国家已将NAL用于环境医学与职业医学...  相似文献   
105.
In this study, we aimed to evaluate the effect of Nobiletin (NOB) on the placenta of Sprague–Dawley (SD) rats that had undergone reduced uterine perfusion pressure (RUPP) surgery and to evaluate the safety of NOB intervention during pregnancy. The results showed that NOB alleviated placental hypoxia, attenuated placental cell apoptosis, and inhibited placental damage in RUPP rats. No side effect of NOB intervention during pregnancy was observed. BeWo cell lines with P53 knockdown were then constructed using lentiviral transfection, and the P53 signaling pathway was found to be essential for NOB to reduce hypoxia-induced apoptosis of the BeWo cell lines. In summary, NOB attenuated hypoxia-induced placental damage by regulating the P53 signaling pathway, and those findings may contribute some insights into the role of NOB in placental development and the prevention of placental-related diseases.  相似文献   
106.
Objectives: The aim of the present work was to comparatively investigate the generation and characteristics of fretting and sliding wear debris produced by CuNiAl against 42CrMo4. Methods: Tribological tests were conducted employing a self-developed tribometer. Most experimental conditions were set the same except for the amplitudes and number of cycles. Morphological, chemical, microstructural and dimensional features of the worn area and debris were investigated using optical microscope (OM), X-ray diffraction (XRD), scanning electron microscopy (SEM) with energy dispersive spectroscopy (EDS) and a laser particle sizer. Outcomes: Not only wear scar profiles but also the wear debris color, distribution and generated amount under fretting and sliding wear modes were quite different, which can be attributed to the significant difference in wear mechanisms. Particle size analysis indicates that the fretting debris has a smaller size distribution range; the biggest detected fretting and sliding wear debris sizes were 141 μm and 355 μm, respectively. Both fretting and sliding debris are mainly composed of copper and its oxides, but the former shows a higher oxidation degree.  相似文献   
107.
Background: Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant that can cause hepatotoxicity. The underlying toxicological mechanism remains to be investigated. Given the critical role of fecal microbiota in liver function, it is possible that fecal microbiota may contribute to the liver toxicity induced by PFOS.Objectives: We aimed to investigate the role of liver-fecal microbiota axis in modulating PFOS-induced liver injury in mice.Methods: Male and female mice were exposed to PFOS or vehicle for 14 d. In this investigation, 16S rDNA sequencing and metabolomic profiling were performed to identify the perturbed fecal microbiota and altered metabolites with PFOS exposure. In addition, antibiotic treatment, fecal microbiota transplantation, and bacterial administration were conducted to validate the causal role of fecal microbiota in mediating PFOS-induced liver injury and explore the potential underlying mechanisms.Results: Both male and female mice exposed to PFOS exhibited liver inflammation and steatosis, which were accompanied by fecal microbiota dysbiosis and the disturbance of amino acid metabolism in comparison with control groups. The hepatic lesions were fecal microbiota-dependent, as supported by antibiotic treatment and fecal microbiota transplantation. Mice with altered fecal microbiota in antibiotic treatment or fecal microbiota transplantation experiments exhibited altered arginine concentrations in the liver and feces. Notably, we observed sex-specific lower levels of key microbiota, including Lactobacillus, Enterococcus, and Akkermansia. Mice treated with specific bacteria showed lower arginine levels and lower expression of the phosphorylated mTOR and P70S6K, suggesting lower activity of the related pathway and mitigation of the pathological differences observed in PFOS-exposed mice.Conclusions: Our study demonstrated the critical role of the fecal microbiota in PFOS-induced liver injury in mice. We also identified several critical bacteria that could protect against liver injury induced by PFOS in male and female mice. Our present research provided novel insights into the mechanism of PFOS-induced liver injury in mice. https://doi.org/10.1289/EHP10281  相似文献   
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